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Terminal renal failure as a contributor to high-sensitivity cardiac troponin T elevations: insights from patients undergoing renal transplantation

Background False cardiac troponin (cTn) elevations from non-cardiac causes are a major concern. We aimed to assess terminal renal failure as a possible non-cardiac cause of elevated high-sensitivity cTnT (hs-cTnT) concentrations using renal transplantation as an in vivo model of rapid restoration of renal function.

Methods We analysed consecutive patients with end-stage renal disease (ESRD) undergoing renal transplantation at a single centre. Patients with perioperative myocardial infarction or injury were excluded. Changes in hs-cTnT and creatinine were measured pretransplant and at four post-transplant intervals (day 1, days 2–5 and days 14–180). A decrease of ≥25% in hs-cTnT within 24 hours post-transplant was deemed evidence of renal clearance recovery.

Results Among 45 patients (median age 67 years, 31% women), the median pretransplant plasma creatinine concentration was 608 μmol/L (IQR 482–830), and fell to 425 μmol/L (IQR 337–619) on day 1289 μmol/L (IQR 201–492) on days 2–5 and 126 μmol/L (IQR 103–191) on days 14–180 (p0.001, p0.001 and p=0.003, respectively). The median pretransplant hs-cTnT concentration was 48 ng/L (IQR 34–70). It fell to 26 ng/L (IQR 15–38; geometric mean of relative change 36%) on day 1 (p0.001) and then remained constant on days 2–5 (26 ng/L (IQR 18–35)) and days 14–180 (25 ng/L (IQR 20–30), p=ns).

ER-100: The “Miracle Cure” For Aging? | Aubrey de Grey

The ER-100 drug candidate reverses aging in mice, and David Sinclair says human trials start soon. Is this a magic pill for aging? Dr. Aubrey de Grey discusses the latest advances in life-extension research.

Our story begins on X, where user “rand_longevity” wrote, “Aging will be reversible in humans within 8 years”, to which Dr. David Sinclair replied, “8 years? After successful non-human primate trials, human age reversal trials are set to begin in 6 months”, later naming the ER-100 drug candidate.

Life Biosciences ER-100 drug candidate leverages partial epigenetic programming using 3 of the 4 Yamanaka factors to promote cellular rejuvenation to a younger state without the loss of cell identity. They believe this will help prevent or reverse age-related diseases at a root level — but they’re not the only organization pursuing life-extension research.

Dr. de Grey’s own research has focused primarily on accumulated side effects from metabolism, embodied in the title of his 1999 book, “The Mitochondrial Free Radical Theory of Aging”.

Dr. de Grey is well-known as one of the top gerontology and life-extension scientists in the world, and his own work has also been successful in extending the lifespan of lab animals. In this program, he discusses his work and some of the key elements of living a longer, healthier life.

DISCLAIMER: This program is a discussion is about ongoing scientific research, and is NOT providing medical advice. Please consult your doctor before starting any supplements, beginning an exercise routine, or undertaking lifestyle changes.

New AI tool learns to read medical images with far less data

A new artificial intelligence (AI) tool could make it much easier—and cheaper—for doctors and researchers to train medical imaging software, even when only a small number of patient scans are available.

The AI tool improves upon a process called medical image , where every pixel in an image is labeled based on what it represents—cancerous or normal tissue, for example. This process is often performed by a highly trained expert, and has shown promise in automating this labor-intensive task.

The big challenge is that deep learning-based methods are data hungry—they require a large amount of pixel-by-pixel annotated images to learn, explained Li Zhang, a Ph.D. student in the Department of Electrical and Computer Engineering at the University of California San Diego. Creating such datasets demands expert labor, time and cost. And for many medical conditions and , that level of data simply doesn’t exist.

Novel radioimmunotherapy eradicates cancer stem cells in ovarian cancer model

A new radioimmunotherapy approach has been shown to successfully eliminate cancer stem cells (CSCs) in preclinical models of ovarian cancer, outperforming the current gold standard. This research, published in the July issue of The Journal of Nuclear Medicine, lays the foundation for further development of radionuclide therapies targeting CSCs, offering renewed hope for more effective treatment options and improved outcomes for patients.

CSCs are highly tumorigenic, self-renewable cells that play a key role in tumor relapse, metastasis, and resistance. Although the clinical significance of eliminating CSCs is clearly recognized and CSC immunotherapies have been examined in preclinical and clinical evaluations, the development of such therapies remains a challenge.

“Radioimmunotherapy enables precise, target-specific delivery of particulate radiation to cancer-associated antigens, while minimizing off-target accumulation and increasing tumor retention and irradiation, which makes it a promising choice for targeting CSCs,” stated Jürgen Grünberg, Ph.D., senior scientist at the Center for Radiopharmaceutical Sciences, Center for Life Sciences at the Paul Scherrer Institute in Villigen, Switzerland.

Researchers harness AI-powered protein design to enhance T-cell based immunotherapies

A paper published in Cell highlights how researchers have leveraged AI-based computational protein design to create a novel synthetic ligand that activates the Notch signaling pathway, a key driver in T-cell development and function.

These so-called soluble Notch agonists can be broadly applied to optimize clinical T-cell production and advance immunotherapy development.

Notch signaling is central to many cellular differentiation processes and is essential in transforming human immune cells into T-cells that target viruses and tumors. But activating Notch signaling in the laboratory has posed a challenge.

Melanoma ‘cellular compass’ discovery could help curb metastasis

Researchers have discovered a protein which is critical for steering melanoma cancer cells as they spread throughout the body. The malignant cells become dependent on this protein to migrate, pointing to new strategies for impeding metastasis.

The protein eIF2A is generally thought to spring into action when a cell is under stress, helping ribosomes launch protein synthesis. But according to a study published in the journal Science Advances, eIF2A has a completely different role in melanoma, helping control movement.

“Malignant cells that metastasize need to make their way through tissues in order to invade proximal or distant organs. Targeting eIF2A could be a new strategy to impede melanoma breaking free and seeding tumors elsewhere,” says Dr. Fátima Gebauer, corresponding author of the study and researcher at the Center for Genomic Regulation (CRG) in Barcelona.

The 0.05% RNA Process That Makes Cancer Self-Destruct

A group of Australian scientists has uncovered a new way to fight some of the toughest cancers by targeting an overlooked cellular process called minor splicing. This tiny but vital mechanism turns out to be essential for the growth of certain tumors, especially those driven by KRAS mutations — a common but hard-to-treat culprit in cancer. By blocking minor splicing, researchers triggered DNA damage and activated the body’s own cancer-defense system, killing cancer cells while sparing healthy ones. The results in animal and human cell models are so promising that drug development is now underway, potentially paving the way for more effective and less toxic treatments across multiple cancer types.

Sugar layer on beta cells prevents immune system from causing type 1 diabetes

Scientific breakthroughs in one disease don’t always shed light on treating other diseases. But that’s been the surprising journey of one Mayo Clinic research team. After identifying a sugar molecule that cancer cells use on their surfaces to hide from the immune system, the researchers have found the same molecule may eventually help in the treatment of type 1 diabetes, once known as juvenile diabetes.

Type 1 diabetes is a chronic autoimmune condition in which the immune system errantly attacks that produce insulin. The disease is caused by genetic and other factors and affects an estimated 1.3 million people in the U.S.

In their studies, the Mayo Clinic researchers took a cancer mechanism and turned it on its head. Cancer cells use a variety of methods to evade , including coating themselves in a known as sialic acid. The researchers found in a preclinical model of type 1 diabetes that it’s possible to dress up beta cells with the same sugar molecule, enabling the immune system to tolerate the cells.

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